Wf. Lam et al., EFFECT OF ACUTE HYPERGLYCEMIA ON BASAL AND BOMBESIN-STIMULATED PANCREATICOBILIARY SECRETION IN HUMANS, Pancreas, 17(2), 1998, pp. 201-207
This study was undertaken to investigate the effect of acute hyperglyc
emia on basal and bombesin-stimulated pancreaticobiliary secretion. Se
ven healthy subjects participated in two experiments performed in rand
om order during normoglycemia and hyperglycemic clamping at 15 mM. Duo
denal outputs of bilirubin, trypsin, amylase, and bicarbonate were mea
sured by aspiration with a recovery marker under basal conditions for
60 min and during continuous infusion of bombesin (1 ng/kg . min) for
60 min. Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) l
evels were determined at regular intervals. Compared to normoglycemia,
during hyperglycemia basal outputs of bilirubin (17 +/- 3 vs. 0.9 +/-
0.4 mu mol/60 min), trypsin (24 +/- 4 vs. 4 +/- 1 U/60 min), amylase
(12 +/- 1 vs. 3 +/- 1 kU/60 min), and bicarbonate (2.9 +/- 0.5 vs. 1.2
+/- 0.2 mmol/60 min) were significantly p < 0.05) reduced. Bombesin s
ignificantly (p < 0.05) increased pancreaticobiliary output during bot
h normo- and hyperglycemia. During hyperglycemia bombesin-stimulated 6
0-min outputs of bilirubin, trypsin, amylase, and bicarbonate were not
significantly different compared to those during normoglycemia. Basal
and bombesin-stimulated plasma PP concentrations were significantly (
p < 0.05) reduced during hyperglycemia, but plasma CCK levels were not
significantly different. It is concluded that acute hyperglycemia red
uces basal but does not affect bombesin-induced pancreaticobiliary sec
retion.